Faculty Opinions recommendation of The pathophysiology of endometriosis and adenomyosis: tissue injury and repair.

Author(s):  
Sun-Wei Guo
1988 ◽  
Vol 63 (S1) ◽  
pp. 28-28a
Author(s):  
D. Nonclercq ◽  
V. Yernaux ◽  
G. Toubeau ◽  
G. Laurent ◽  
J.A. Heuson-Stiennon

2019 ◽  
Author(s):  
Kathleen E. DelGiorno ◽  
Chi-Yeh Chung ◽  
Raj Giraddi ◽  
Eugene Ke ◽  
H. Carlo Maurer ◽  
...  

This resource will be invaluable to those clinicians who are involved with, or anticipate involvement with, sports people and those exercising for health benefits or for pleasure, many of whom will be in need of expert advice following injury. It is organised by anatomical region and by sport, and also covers basic sciences such as functional anatomy, tissue injury and repair, and principles of examination and treatment to further enhance understanding.


2020 ◽  
Vol 9 (2) ◽  
pp. 485 ◽  
Author(s):  
Guo

Adenomyosis is used to be called endometriosis interna, and deep endometriosis is now called adenomyosis externa. Thus, there is a question as to whether adenomyosis is simply endometriosis of the uterus, either from the perspective of pathogenesis or pathophysiology. In this manuscript, a comprehensive review was performed with a literature search using PubMed for all publications in English, related to adenomyosis and endometriosis, from inception to June 20, 2019. In addition, two prevailing theories, i.e., invagination—based on tissue injury and repair (TIAR) hypothesis—and metaplasia, on adenomyosis pathogenesis, are briefly overviewed and then critically scrutinized. Both theories have apparent limitations, i.e., difficulty in falsification, explaining existing data, and making useful predictions. Based on the current understanding of wound healing, a new hypothesis, called endometrial-myometrial interface disruption (EMID), is proposed to account for adenomyosis resulting from iatrogenic trauma to EMI. The EMID hypothesis not only highlights the more salient feature, i.e., hypoxia, at the wounding site, but also incorporates epithelial mesenchymal transition, recruitment of bone-marrow-derived stem cells, and enhanced survival and dissemination of endometrial cells dispersed and displaced due to iatrogenic procedures. More importantly, the EMID hypothesis predicts that the risk of adenomyosis can be reduced if certain perioperative interventions are performed. Consequently, from a pathogenic standpoint, adenomyosis is not simply endometriosis of the uterus, and, as such, may call for interventional procedures that are somewhat different from those for endometriosis to achieve the best results.


Author(s):  
Jack Antel

ABSTRACT:All currently approved therapies for multiple sclerosis (MS) modulate systemic immune components prior to their entry into the central nervous system (CNS). Available data indicate they lack impact on the progressive phases of disease; the more potent systemic immune-directed agents predispose to development of infectious or neoplastic disorders. Development of new agents that enhance disease stage related efficacy and limit systemic toxicity will need to consider the underlying mechanisms related to each phase of the clinical disorder, namely relapses, remission, and progression. This report focuses on disease related mechanisms ongoing within the CNS that contribute to the different phases of MS and how these may serve as potential therapeutic targets. Such mechanisms include CNS compartment specific immunologic properties especially as related to the innate immune system and neural cell-related properties that are determinants of the extent of actual tissue injury and repair (or lack thereof).


2011 ◽  
Vol 91 (1) ◽  
pp. 221-264 ◽  
Author(s):  
Dianhua Jiang ◽  
Jiurong Liang ◽  
Paul W. Noble

Accumulation and turnover of extracellular matrix components are the hallmarks of tissue injury. Fragmented hyaluronan stimulates the expression of inflammatory genes by a variety of immune cells at the injury site. Hyaluronan binds to a number of cell surface proteins on various cell types. Hyaluronan fragments signal through both Toll-like receptor (TLR) 4 and TLR2 as well as CD44 to stimulate inflammatory genes in inflammatory cells. Hyaluronan is also present on the cell surface of epithelial cells and provides protection against tissue damage from the environment by interacting with TLR2 and TLR4. Hyaluronan and hyaluronan-binding proteins regulate inflammation, tissue injury, and repair through regulating inflammatory cell recruitment, release of inflammatory cytokines, and cell migration. This review focuses on the role of hyaluronan as an immune regulator in human diseases.


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